Sodium selenite promotes neurological function recovery after spinal cord injury by inhibiting ferroptosis

• Published in: Neural regeneration research Vol. 17; no. 12; pp. 2702 - 2709
• Main Authors: Chen, Yi-Xin, Zuliyaer, Talifu, Liu, Bin, Guo, Shuang, Yang, De-Gang, Gao, Feng, Yu, Yan, Yang, Ming-Liang, Du, Liang-Jie, Li, Jian-Jun
• Format: Journal Article
• Language: English
• Published: India Wolters Kluwer India Pvt. Ltd 01.12.2022; Medknow Publications & Media Pvt. Ltd; Center of Neural Injury and Repair,Beijing Institute for Brain Disorders,Beijing,China; Beijing Key Laboratory of Neural Injury and Rehabilitation,Beijing,China; China Rehabilitation Science Institute,Beijing,China; Beijing Key Laboratory of Neural Injury and Rehabilitation,Beijing,China%Department of Spine Surgery,Hunan Provincial People's Hospital(The First Affiliated Hospital of Hunan Normal University),Changsha,Hunan Province,China%China Rehabilitation Science Institute,Beijing,China; Department of Spinal and Neural Functional Reconstruction,China Rehabilitation Research Center,Beijing,China; School of Rehabilitation Medicine,Capital Medical University,Beijing,China; Department of Rehabilitation Medicine,Xiangya Hospital of Central South University,Changsha,Hunan Province,China%School of Rehabilitation Medicine,Capital Medical University,Beijing,China; Wolters Kluwer - Medknow; Wolters Kluwer Medknow Publications
• Subjects: Ferroptosis; ferroptosis; glutathione peroxidase 4; glutathione; iron; lipid peroxidation; neural regeneration; secondary injury; sodium selenite; specificity protein 1; spinal cord injury; Proteins; Sodium; Spinal cord injuries; spinal cord injury; glutathione peroxidase 4; ferroptosis; neural regeneration; secondary injury; sodium selenite; specificity protein 1; glutathione; iron; lipid peroxidation
• ISSN: 1673-5374; 1876-7958
• DOI: 10.4103/1673-5374.339491

Ferroptosis is a recently discovered form of iron-dependent cell death, which occurs during the pathological process of various central nervous system diseases or injuries, including secondary spinal cord injury. Selenium has been shown to promote neurological function recovery after cerebral hemorrhage by inhibiting ferroptosis. However, whether selenium can promote neurological function recovery after spinal cord injury as well as the underlying mechanism remain poorly understood. In this study, we injected sodium selenite (3 µL, 2.5 µM) into the injury site of a rat model of T10 vertebral contusion injury 10 minutes after spinal cord injury modeling. We found that sodium selenite treatment greatly decreased iron concentration and levels of the lipid peroxidation products malondialdehyde and 4-hydroxynonenal. Furthermore, sodium selenite increased the protein and mRNA expression of specificity protein 1 and glutathione peroxidase 4, promoted the survival of neurons and oligodendrocytes, inhibited the proliferation of astrocytes, and promoted the recovery of locomotive function of rats with spinal cord injury. These findings suggest that sodium selenite can improve the locomotive function of rats with spinal cord injury possibly through the inhibition of ferroptosis via the specificity protein 1/glutathione peroxidase 4 pathway.